Cardiology

We present a case of an intermediate coronary artery stenosis with concomitant severe mitral regurgitation, in which hyperemic efficacy of intravenous (IV) infusion of adenosine was initially blunted and was completely restored by surgical correction of the diseased valve. As the half-life of adenosine is extremely short, any conditions resulting in a low cardiac output state may hinder the accumulation of serum adenosine given intravenously enough to induce maximal hyperemia. In this situation, alternative methods to increase IV infusion rate or switch to intracoronary injection may be advisable.

BACKGROUNDWe evaluated the predictive ability of cystatin C and creatinine-based estimations of glomerular filtration rate (eGFR), including the Chronic Kidney Disease–Epidemiology (CKD-EPI) equation, in acute coronary syndrome (ACS) patients with (STE-ACS) or without (NSTE-ACS) ST elevation in a large contemporary ACS population.METHODSConcentrations of cystatin C and creatinine, as well as eGFR at randomization, were measured in 16 401 patients in the Platelet Inhibition and Patient Outcomes (PLATO) study and evaluated as predictors of the composite end point of cardiovascular death or myocardial infarction within 1 year. Two Cox proportional hazards models were used, the first adjusting for clinical characteristics and the second for clinical characteristics plus the biomarkers N-terminal pro–B-type natriuretic peptide, troponin I, and C-reactive protein.RESULTSThe median cystatin C value was 0.83 mg/L. Increasing quartiles of cystatin C were strongly associated with poor outcome...

Background— Reduced renal function is associated with a poorer prognosis and increased bleeding risk in patients with acute coronary syndromes and may therefore alter the risk-benefit ratio with antiplatelet therapies. In the Platelet Inhibition and Patient Outcomes (PLATO) trial, ticagrelor compared with clopidogrel reduced the primary composite end point of cardiovascular death, myocardial infarction, and stroke at 12 months but with similar major bleeding rates. Methods and Results— Central laboratory serum creatinine levels were available in 15 202 (81.9%) acute coronary syndrome patients at baseline, and creatinine clearance, estimated by the Cockcroft Gault equation, was calculated. In patients with chronic kidney disease (creatinine clearance <60 mL/min; n=3237), ticagrelor versus clopidogrel significantly reduced the primary end point to 17.3% from 22.0% (hazard ratio [HR], 0.77; 95% confidence interval [CI], 0.65 to 0.90) with an absolute risk reduction greater than that...

Background: Cystatin C levels reflects glomerular filtration rate and predict cardiovascular mortality and morbidity in coronary artery disease. Our aim was to determine the predictive power of cystatin C in patients with STEMI as well as in NSTE-ACS. Methods: Cystatin C measured at randomization in 16402 (of 18624 included) patients in the PLATO study (6638 STEMI and 9764 suspected NSTE-ACS) was evaluated as a predictor of the composite endpoint of cardiovascular death or myocardial infarction (MI) within one year. Cystatin C was evaluated as a continuous variable (logarithmized), as quartiles and dichotomized at optimal cutoff using the Integrated Discrimination Improvement (IDI) measure. Two Cox proportional hazards models were used: 1/ established traditional risk factors (e.g. age, gender, heart failure, diabetes, BMI, randomized treatment) and 2/ above mentioned and the addition of further risk markers e.g. NT-proBNP and CRP. The median cystatin C value was 0.77 mg/L in the STEMI group and 0.86 mg/L in the NSTE-ACS group. The hazard ratios for the continuous models were derived per standard deviation 0.35 log(mg/L). The optimal cutoff was 1.09 mg/L. There was no significant cystatin C by type of ACS interaction (STEMI or NSTE-ACS).

Objective To test the a priori hypothesis that the association between cold spells and ischaemic sudden cardiac death (SCD) is modified by the severity of coronary stenosis. Methods The home coordinates of 2572 autopsy-verified cases of ischaemic SCD aged ≥35 in the Province of Oulu, Finland, were linked to 51 years of weather data. Cold spell was statistically defined for each home address as unusually cold weather pertinent to the location and time of year. We estimated the occurrence of cold spells during the hazard period (7 days preceding death) and reference periods (the same calendar days over 51 years) in a casecrossover setting applying conditional logistic regression, controlling for temporal trends and stratifying by severity of coronary stenosis. results The association between cold spells and ischaemic SCD was stronger among patients with 75%-95% stenosis (OR 2.03; 95% CI 1.31 to 3.17), and weaker to non-existent among patients with <75% stenosis (OR 0.97; 95% CI 0.37 to 2.55) or coronary total occlusion (100% stenosis) (OR 1.01; 95% CI 0.52 to 1.96). Lack of calcium-channel blockers and statin therapy seemed to accentuate the role of stenosis during cold spells. Conclusions We provide evidence that the association between cold spells and ischaemic SCD is modified by the severity of coronary stenosis. The findings suggest that disturbances in coronary circulation play part in the pathogenesis of SCD during cold weather.

Objective: We examined the endothelial nitric oxide (eNOS) gene Glu298Asp polymorphism to assess its possible association with the extent of coronary collaterals. Methods: A total of 473 consecutive patients who had high grade coronary stenosis or occlusion were evaluated for the extent of coronary collaterals by using Rentrop classification. Patients with grade 0 or 1 collaterals were identified as having poor collaterals. The relation between collateral status and eNOS Glu298Asp polymorphism was studied by multivariate logistic regression analysis. Results: Subjects with poor collaterals were more likely to have diabetes mellitus (p < 0.001) and unstable angina pectoris as clinical presentation (p = 0.014) and more likely to carry Asp298 variant (p = 0.02) but they were less likely to have received statins (p = 0.031). Multivariate analysis demonstrated that Asp298 allele carriers were 1.7 times more likely to have poor collaterals than patients with GluGlu genotype (95% CI: 1.09-2.69, p = 0.024). There was a significant interaction between diabetes mellitus and eNOS Glu298Asp polymorphism in the analysis of collateral development. Among 145 diabetic patients Asp298 allele was the only predictor of poor collateral development with OR of 5.38 (95% CI: 2.41-11.98, p < 0.001). Once diabetic patients were excluded from the analysis Asp298 allele was no longer a significant correlate of poor collateral formation. Conclusions: The present study suggests that the Asp298 allele of the eNOS gene is significantly associated with impaired collateral development, especially in patients with diabetes mellitus. Treatment strategies that modulate eNOS activity and/or NO production may improve coronary collateral development.

Introduction: Hypertrophic cardiomyopathy (HCM) is characterized by disorganized myocardial architecture, and may cause ventricular arrhythmias and sudden death. The angiotensin-converting enzyme (ACE) with two deletion alleles (DD genotype) has been proposed to be associated with increased myocardial collagen content. We evaluated QT dispersion (QTd), which reflects regional differences in ventricular repolarization, in HCM patient and controls among the three different ACE genotypes. Materials and methods: Sixty-three patients with HCM and 20 healthy subjects were included in the study. QT parameters were measured from 12 lead electrocardiograms. ACE genotypes were determined from the DNA extracted from peripheral blood by a polymerase chain reaction (PCR) method. QT parameters were compared among the three ACE genotypes both in HCM patients and controls. Results: Median ages were similar in HCM and control groups. QTd and corrected QTd (QTcd) were significantly greater in the HCM group compared with the controls. The frequencies of each genotype were similar in both groups. Although QTd and QTcd did not differ among the three genotypes in the control subjects, they were significantly greater in patients with DD genotype compared with other genotypes in the HCM group. Conclusion: QTd and QTcd are increased in patients with HCM, especially in those with the DD genotype.

Background Coronary artery abnormalities in Kawasaki disease (KD) are assessed using echocardiographic z-scores. We hypothesized that changing the coronary artery (CA) z-score model would alter diagnosis and management of children with KD. Methods In this retrospective single-center study of children treated for KD (9/2007-1/2020), we collected echocardiographic measurements for the left anterior descending (LAD), right (RCA), and left main (LMCA) coronary arteries during 3 illness phases and calculated Boston and Pediatric Heart Network (PHN) z-scores. Agreement between Boston and PHN z-scores was assessed using Kappa (κ) and Lin's Concordance Correlation Coefficients (CCC) and Bland-Altman analysis. Results For 904 echocardiograms from 357 children, the median Boston LAD z-score was lower than the PHN (0.3 [IQR -0.6, 1.5] vs 1.6 [IQR 0.7, 2.8], CCC 0.94 [95% CI 0.93, 0.95], moderate agreement), aggregated across all illness phases. RCA and LMCA z-scores showed substantial agreement. With conversion from Boston to PHN models, the percentage of individual LAD z-scores ≥ 2.5 increased (14.6% to 32.1%). At least one CA z-score classification changed in 213 children (59.7%) across all phases, and 48 children (13.4%) had a change that altered recommended antithrombotic strategy. Agreement between models differed by age, sex, and race. Conclusions Conversion from Boston to PHN z-scores changed at least 1 CA z-score classification in over half of KD patients and changed recommended antithrombotic management in 13%, largely driven by LAD measurements. Since diagnosis and management of KD and KD-like diseases rely upon CA z-scores, the clinical and research implications of these findings merit further exploration.

Children with dilated cardiomyopathy awaiting transplantation who fail maximal pharmacologic therapy may benefit from intra-aortic balloon pumping. Between July 1993 and August 1999, a total of 4 children with dilated cardiomyopathy underwent pre-transplant balloon pumping for 6.0 Ϯ 5.8 (1 to 12) days. One child (pumped for 12 days) died awaiting transplant, and the remaining 3 were successfully transplanted. Intra-aortic balloon pumping timed precisely with M-mode echocardiographic markers offers a relatively simple and safe intermediate level of mechanical support for children with dilated cardiomyopathy who fail pharmacologic support.

Objectives: Although previous studies in dogs have indicated a minimal role for changes in I K1 in the shortening of action potential duration (APD) associated with atrial fibrillation (AF), in humans, there is evidence for significant AF-induced up-regulation of this current. In this computer model study, we investigated the relative contributions of the remodeling of I K1 , L-type calcium current, and other remodeled ionic channel currents to AF-induced APD reduction in human atrium. Methods: Two computer models of electrical activity of human atrial cell were modified by incorporating experimental data of AF-induced changes in human atrial ionic channel conductance and kinetics reported by Bosch et al. (I CaL , I to , I K1 , and I Na ) (AF-1) and Workman et al. (I CaL , I to , and I K1 ) (AF-2). The roles and relative importance of individually remodeled ion channels in the APD reduction in human atrium were evaluated by the removal and exclusive methods, in which remodeling of specific currents was omitted, or considered in isolation, in the two models. Results: When tested together, previously reported AF-induced changes in sarcolemmal ion currents result in marked shortening of atrial APD 90 . With the AF-1 remodeled parameters, there is a 62% reduction in APD 90 for the Nygren et al. model, and a 68% reduction for the Courtemanche et al. model, which are comparable to experimental results of 60% reduction seen in humans. When tested individually, AF-1-induced changes in I CaL , I K1 , or I to alone result in APD 90 reduction of 20%, 64%, and À10%, respectively, for the Nygren et al. model, and 27%, 40%, and 11.6%, respectively, for the Courtemanche et al. model. With the AF-2 remodeled parameters, there is a 47% reduction in APD 90 for the Nygren et al. model and a 49% reduction for the Courtemanche et al. model, which are also comparable to experimental results of 45% reduction. When tested individually, AF-2-induced changes in I CaL or I K1 alone result in APD 90 reduction of 20% and 40%, respectively, for the Nygren et al. model, and 14% and 21%, respectively, for the Courtemanche et al. model. Conclusion: Previously reported changes in L-type Ca 2+ current are insufficient to account for the observed reduction in atrial APD associated with persistent AF. Up-regulation of I K1 has a greater influence on atrial APD in the human model.

Changes in action potentials of atrial myocytes and various ionic channels induced by chronic atrial fibrillation (AF) have been described in the human. The mechanisms underlying the AF-induced action potential duration (APD) shortening have not been clearly identified. In this study we modify two different computational models of electrical activity of human atrial myocytes by incorporating chronic AF induced changes in several of the ionic channels systems found in myocytes. We examine the ionic mechanisms underlying the AF induced APD reduction and the relative roles of different remodeled ionic channels in producing the APD reduction. In both models we have found that AF induced changes in the ionic channel conductances and kinetics are able to reproduce the APD reduction seen experimentally. AF-induced down regulation of L-type Ca current is insufficient to account for the observed APD reduction, but up regulation of I/sub Kl/ has a much greater influence.

There are two possible mechanisms: abnormal spontaneous electrical activity of ectopic foci and multiple re-entrant wavelets. In this study, we developed a biophysically detailed computer model of virtual human atrium to study the interaction between the two major arrhythmic origins. Depending on their frequencies, phases and distance, the interaction is competitive with either ectopic focus or reentry dominating atrial electrical excitation. Collisions between the two lead to further wave-breaks and the formation of multiple reentrant wavelets, providing a source for persistent atrial fibrillation. Focal activity acting as an organising centre, or mother motor which drives and controls the rhythm of reentry was observed.

The idea of this research is to determine can we tell from the HRV data without paroxysmal atrial fibrillation present at the recording if the patient suffers from this arrhythmia. The benefit is we can provide time and cost effective preliminary screening procedure during short time visit to the clinic. To achieve this goal we used Fourier analysis of the 30 minute HRV segment duration. We found statistically significant increase in the energy above 0.1Hz for the patients with documented PAF history. This suggests that people with this arrhythmia has increased parasympathetic activity. For automatic classification of the patient we trained artificial neural networks on the HRV Fourier spectrum of AFPDB database. Testing on the AFDB (66.5 hours of HRV data from PAF patients) and NSRDB (352 hours of HRV data from healthy ones) databases produced Se 94.5% and Sp 96.5%.

Objectives: Although previous studies in dogs have indicated a minimal role for changes in I K1 in the shortening of action potential duration (APD) associated with atrial fibrillation (AF), in humans, there is evidence for significant AF-induced up-regulation of this current. In this computer model study, we investigated the relative contributions of the remodeling of I K1 , L-type calcium current, and other remodeled ionic channel currents to AF-induced APD reduction in human atrium. Methods: Two computer models of electrical activity of human atrial cell were modified by incorporating experimental data of AF-induced changes in human atrial ionic channel conductance and kinetics reported by Bosch et al. (I CaL , I to , I K1 , and I Na ) (AF-1) and Workman et al. (I CaL , I to , and I K1 ) (AF-2). The roles and relative importance of individually remodeled ion channels in the APD reduction in human atrium were evaluated by the removal and exclusive methods, in which remodeling of specific currents was omitted, or considered in isolation, in the two models. Results: When tested together, previously reported AF-induced changes in sarcolemmal ion currents result in marked shortening of atrial APD 90 . With the AF-1 remodeled parameters, there is a 62% reduction in APD 90 for the Nygren et al. model, and a 68% reduction for the Courtemanche et al. model, which are comparable to experimental results of 60% reduction seen in humans. When tested individually, AF-1-induced changes in I CaL , I K1 , or I to alone result in APD 90 reduction of 20%, 64%, and À10%, respectively, for the Nygren et al. model, and 27%, 40%, and 11.6%, respectively, for the Courtemanche et al. model. With the AF-2 remodeled parameters, there is a 47% reduction in APD 90 for the Nygren et al. model and a 49% reduction for the Courtemanche et al. model, which are also comparable to experimental results of 45% reduction. When tested individually, AF-2-induced changes in I CaL or I K1 alone result in APD 90 reduction of 20% and 40%, respectively, for the Nygren et al. model, and 14% and 21%, respectively, for the Courtemanche et al. model. Conclusion: Previously reported changes in L-type Ca 2+ current are insufficient to account for the observed reduction in atrial APD associated with persistent AF. Up-regulation of I K1 has a greater influence on atrial APD in the human model.

In both human and animal mammals, the pacemaker of the heart, the sinoatrial node (SA node), deteriorates with age. The main features of the aged SA nodes are a slow pacemaking rate and possible SA node-atrium conduction exit block or arrest of SA node pacemaking (i.e., termination of the SA node pacemaker activity). The mechanisms underlying the age-related dysfunction of the heart are unclear. In this study, we developed a detailed computer model of normal and aged SA nodes. Using the model we evaluated the functional roles of age-dependent reduction in SA node i Na current and active cell population in initiation and conduction of pacemaker activity in the aged heart. Simulations have shown that decrease in the SA node i Na or active cell population results in an increase of pacemaking cycle length (equivalent to a decrease of pacemaking rate) and slowing down of SA node-atrium conduction. It also produces the SA node-atrium conduction block in which action potentials originating from the SA node can fail to conduct into the atrium, or termination of the SA node pacemaker activity. When considered together, combined actions have a greater impact on weakening the pacing and driving ability and producing impairment of impulse initiation and conduction that leads to the SA nodeatrium conduction exit block. These simulations provide mechanistic insights for understanding the dysfunction of the SA node in aged hearts.

Voltage-dependent sodium (Na+) channels are heterogeneously distributed through the pacemaker of the heart, the sinoatrial node (SA node). The measured sodium channel current ( iNa) density is higher in the periphery but low or zero in the center of the SA node. The functional roles of iNa in initiation and conduction of cardiac pacemaker activity remain uncertain. We evaluated the functional roles of iNa by computer modeling. A gradient model of the intact SA node and atrium of the rabbit heart was developed that incorporates both heterogeneities of the SA node electrophysiology and histological structure. Our computations show that a large iNa in the periphery helps the SA node to drive the atrial muscle. Removal iNa from the SA node slows down the pacemaking rate and increases the sinoatrial node-atrium conduction time. In some cases, reduction of the SA node iNa results in impairment of impulse initiation and conduction that leads to the SA node-atrium conduction exit block. Dec...

The rising incidence of non-ST-segment elevation myocardial infarction (NSTEMI) and associated long-term high mortality constitutes an urgent clinical issue. Unfortunately, the study of possible interventions to treat this pathology lacks a reproducible pre-clinical model. Indeed, currently adopted small and large animal models of MI mimic only fullthickness, ST-segment-elevation (STEMI) infarcts, and hence cater only for investigation into therapeutics and interventions directed at this subset of MI. Thus, we developed an ovine model of NSTEMI by ligating the myocardial muscle at precise intervals parallel to the left anterior descending coronary artery. After validating the presented model both by histology and functional analysis with clinical data, further omics analyses highlighted the distinctive features of post-NSTEMI tissue remodelling. Here, by looking at the transcriptome and proteome-derived pathways emerging at acute (7 days) and late (28 days) post-surgery timepoints, we discovered specific alterations in cardiac post-ischaemic extracellular matrix (ECM). Together with the rise of well-known markers of inflammation and fibrosis, NSTEMI ischaemic regions showed distinctive patterns in the expression of complex N-glycans and glycosaminoglycans in cellular membranes and ECM. Identifying such changes in molecular moieties accessible to infusible and intra-myocardial injectable drugs sheds light on the development of targeted pharmacological solutions to contrast adverse fibrotic remodelling.

Background: In the assessment of patients with chest pain, there is support for the use of pre-hospital ECG in the literature and in the care guidelines. Using propensity score methods, we aim to examine whether the mere acquisition of a pre-hospital ECG among patients with chest pain affects the outcome (30-day mortality). Methods: The association between pre-hospital ECG and 30-day mortality was studied in the overall cohort (n = 13151), as well as in the one-to-one matched cohort with 2524 patients not examined with pre-hospital ECG and 2524 patients examined with pre-hospital ECG. Results: In the overall cohort, 21% (n = 2809) did not undergo an ECG tracing in the pre-hospital setting. Among those who had pain during transport, 14% (n = 1159) did not undergo a pre-hospital ECG while 32% (n = 1135) of those who did not have pain underwent an ECG tracing. In the overall cohort, the OR for 30-day mortality in patients who had a pre-hospital ECG, as compared with those who did not, was 0.63 (95% CI 0.05-0.79; p b 0.001). In the matched cohort, the OR was 0.65 (95% CI 0.49-0.85; p b 0.001). Using the propensity score, in the overall cohort, the corresponding HR was 0.65 (95% CI 0.58-0.74). Using propensity score methods, we provide real-world data demonstrating that the adjusted risk of death was considerably lower among the cases in whoma pre-hospital ECG was used. The PH-ECG is underused among patients with chest discomfort and the mere acquisition of a pre-hospital ECG may reduce mortality.

To evaluate whether a computer-based decision support system could improve the allocation of patients with acute coronary syndrome (ACS) or a life-threatening condition (LTC). We hypothesised that a system of this kind would improve sensitivity without compromising specificity. A total of 2285 consecutive patients who dialed 112 due to chest pain were asked 10 specific questions and a prediction model was constructed based on the answers. We compared the sensitivity of the dispatchers&#39; decisions with that of the model-based decision support model. A total of 2048 patients answered all 10 questions. Among the 235 patients with ACS, 194 were allocated the highest prioritisation by dispatchers (sensitivity 82.6%) and 41 patients were given a lower prioritisation (17.4% false negatives). The allocation suggested by the model used the highest prioritisation in 212 of the patients with ACS (sensitivity of 90.2%), while 23 patients were underprioritised (9.8% false negatives). The resu...

Objective-To measure the length of time spent discussing all aspects of new prescriptions and guideline-recommended aspects of counseling, and to evaluate factors associated with duration of discussion. Methods-We analyzed tape recordings in which 181 patients received 234 new medication prescriptions from 16 family physicians, 18 internists, and 11 cardiologists in 2 healthcare systems in Sacramento, California between January and November 1999. Results-Of the mean total visit time of 15.9 minutes (SD=434 seconds), a mean of 26 seconds (SD=28 seconds) was allocated to guideline-recommended components and a mean of 23 seconds (SD=25 seconds) was allocated to discussion of all other aspects of new prescription medications. The majority of time spent discussing individual new prescriptions was dedicated to: medication purpose or justification, directions and duration of use, and side effects. On average, more complete discussion of these components was associated with more time. More time was spent talking about guideline-recommended information if patients were in better health, if there was a third party in the room, and if the medication belonged to a psychiatric, compared to an ear, nose, throat medication class. Less time was spent discussing over-the-counter medications and those prescribed to patients with a previous visit to the physician. medications requires more time, and may be difficult to achieve in short office visits. Practice Implications-Time-compressed office visits may need to be redesigned to promote improved provider-patient communication about new medications.

Background: Communication about taking a new medication is critical to proper use of drug therapy and to patient adherence. Despite ample evidence that medications are not taken as prescribed, few investigations have detailed the elements of communication about new medication therapy. This article describes and assesses the quality of physician communication with patients about newly prescribed medications. This was an observational study that combined patient and physician surveys with transcribed audiotaped office visits from 185 outpatient encounters with 16 family physicians, 18 internists, and 11 cardiologists in 2 Sacramento, Calif, health care systems between January and November 1999, in which 243 new medications were prescribed. We measured the quality of physician communication when prescribing new medications. Results: Physicians stated the specific medication name for 74% of new prescriptions and explained the purpose of the medication for 87%. Adverse effects were addressed for 35% of medications and how long to take the medication for 34%. Physicians explicitly instructed 55% of patients about the number of tablets to take and explained the frequency or timing of dosing 58% of the time. Physicians fulfilled a mean of 3.1 of 5 expected elements of communication when initiating new prescriptions. They counseled the most about psychiatric medications, fulfilling a mean of 3.7, 3.5, and 3.4, pulmonary, and cardiovascular elements, respectively. Conclusions: When initiating new medications, physicians often fail to communicate critical elements of medication use. This might contribute to misunderstandings about medication directions or necessity and, in turn, lead to patient failure to take medications as directed.

Atherosclerosis is a build-up of low-density lipoproteins (LDL) in the channels of blood vessels. This occludes the vessels and, occurring in the carotid arteries, portends conditions that favour stroke. This work is an attempt to mathematically represent the physiological process of atherosclerosis caused by plaques on the walls of the human arteries. Provide insight into the effect of blood flow velocity on wall shear stress and its implications on atherosclerosis progression in a human carotid artery via computational simulation. The effect of blood velocity on plaque growth and progression is simulated using COMSOL multi-physics. The human carotid was modeled in 2-D with Stokes law for model flow. The simulation began with a plaque-free vessel with velocities of 30 m/s -125 m/s. Results showed that the rate of plaque initiation dropped as the blood velocity increased from 30 m/s to 125 m/s; higher inlet velocities gave lower plaque growth; the highest degree of 30% stenosis was recorded at a blood velocity of 30 m/s. Plaque height significantly

Background: This study aimed to assess the factors contributing to the outcomes of recently hospitalized patients with heart failure (HF). Methods: A prospective data of 76 adults who were admitted due to acute HF between October 1, 2019 and June 30, 2020 at our center were analyzed. Endpoints included survival and rehospitalization within six months after discharge. Results: The mean age was 64.9 ± 13.8 years, with a male preponderance (68.4%). Approximately 60.5% of patients had the left ventricular ejection fraction (LVEF) <40%, whereas 26.3% of patients had LVEF ≥50%. Coronary artery disease (75%), arterial hypertension (72.4%), chronic kidney disease (46.1%), and diabetes mellitus (46.1%) were the most frequent comorbidities. Poor compliance (40.8%) and non-cardiac infection (21.1%) were the common precipitating factors for hospitalization. The majority of subjects had severe symptoms, indicated by the frequent need of intensive care unit (43%), high N-terminal prohormone brain natriuretic peptide levels [NT-proBNP; median, 4765 (1539.7-11782.2) pg/mL], and presence of either atrial fibrillation, severe mitral regurgitation, or significant pulmonary hypertension in approximately one-third of cases. Even though in-hospital mortality was relatively low (2.6%), the all-cause mortality and rehospitalization rates in the next six months after discharge were still high, reaching 22.54% and 19.72%, respectively. Further survival analysis showed that tachycardia on admission and pre-existing chronic kidney disease (CKD) resulted in low six-month survival rates among these patients. Conclusion: After hospital discharge, patients with HF were still exposed to higher risks of death and readmission albeit with the medication addressed. Tachycardia on admission and pre-existing CKD might predict worse outcomes.

Background: Cardiovascular diseases are the second leading cause of morbidity and mortality in Kenya. However, there is limited clinico-epidemiological data on stroke to inform decision making. This study sought to establish stroke distribution patterns and characteristics in patients seeking care at Kenyatta National Hospital (KNH) and Moi Teaching and Referral Hospital (MTRH), with the ultimate aim of establishing the first national stroke registry in Kenya. Methods: This was a prospective multicentre cohort study among stroke patients. The study used a modified World Health Organisation STEP-wise approach to stroke surveillance tool in collecting data on incidence, major risk factors and mortality rate. The Cochran's Mantel-Haenszel chisquared test of conditional independence was used with p-value set at 0.05. Results: A total of 691 patients with confirmed stroke were recruited [KNH 406 (males: 40.9%; females: 59.1%); MTRH 285 (males: 44.6%; females: 55.4%)] and followed over a 12-month period. Overall, ischaemic stroke accounted for 55.6% of the stroke cases, with women being the most affected (57.5%). Mortality rate at day 10 was 18.0% at KNH and 15.5% at MTRH, and higher in the haemorrhagic cases (20.3%). The most common vascular risk factors were hypertension at 77.3% (males: 75.7%; females: 78.5%), smoking at 16.1% (males: 26.6%; females: 8.3%) and diabetes at 14.9% (males: 15.7%; females: 14.4%). Ischaemic stroke was conditionally independent of gender after adjusting for age. Conclusions: To our knowledge this is the first pilot demonstration establishing a stroke registry in sub-Saharan Africa and clearly establishes feasibility for this approach. It also has utility to both inform and potentially guide public policy and public health measures on stroke in Kenya. Important and unexpected observations included the preponderance of women affected by cerebrovascular disease and that cigarette smoking was the second most common risk factor. The latter, over time, will further impact on the clinico-epidemiological profile of cerebrovascular disease in Kenya.

is hypertensive, and only three out of seven, among the patients that are being treated, are getting the appropriate pharmacotherapy. Our goal is the evaluation and comparison of the pharmacotherapy of adult hospitalized and ambulatory hypertensive population. The cross-sectional, observational, prospective, pharmaco-epidemiological study targets the observation, analysis and comparison of pharmacotherapy of two groups of patients (hospitalized and ambulant patients), in the perspective of polypragmasy and self-medication, if it occured. The average age of hospitalized patients was 70.65+/-4.95 (SD) years, and 68.39+/-10.49 (SD) years of the outpatients. A statistically significant difference has been found regarding the gender rate in the two groups of patients (p = 0.0474), whereas 59% of the hospitalized patients were women compared to only 45% of the outpatients. A statistically significant difference has been found between the two groups' angiotensin convertase enzyme inhibitors (ACEI) use: 44.86% in case of inpatients and 70.52% in case of outpatients (p = 0.0006), and also regarding the usage of beta-receptor blockers (63.83% hospitalized vs. 44.5% ambulatory). The incidence of polypragmasy of inpatients was 85.12% and in 4.26% of the cases a combination of more than ten drugs occurred. Compared to the ambulatory patients, where the incidence rate of polypragmasy was 61.84% and 6.93% of them used more than ten different drugs daily, the difference is statistically significant (p = 0.0004). Female hypertensive patients are more likely to be hospitalized due to their complications. Beta-receptor blockers are more frequently used in hospitalized cases, and ACEI are more widespread in case of ambulatory patients. A possible explanation includes that the use of ACEI is safer and produce less side effects than beta-blockers, which are tested on hospitalized patients before the long-term introduction in their therapy. Polypragmasy is common in both groups of patients, but it seems to occur at higher rates in case of inpatients, due to the more intense monitoring possibilities.

Transcatheter aortic valve implantation (TAVI) is now established as the standard treatment for symptomatic severe aortic stenosis (AS) in patients at high or prohibitive surgical risk, and the preferred treatment for those at intermediate risk. Based on recent trials in low-risk patients, the indications for TAVI are expanding towards the lower-risk classes, and the procedure has even been discussed for younger and asymptomatic patients. 2,3 Although a significant reduction in periprocedural morbidity and mortality has been observed for TAVI over the past decade due to better patient selection, device design and operator experience, the occurrence of periprocedural conduction disturbances remains a concern. The most common post-TAVI conduction abnormalities are left bundle branch block (LBBB) and high-degree atrioventricular block (HAVB) requiring pacemaker implantation (PMI). Although the clinical effects of new-onset LBBB and PMI after TAVI remain controversial, substantial evidence supports an association of these conduction abnormalities with adverse effects. With an expanding indication for TAVI, the possible deleterious consequences of LBBB and PMI need to be taken into account and further clarified. We review the current evidence in conduction abnormalities after TAVI and how to manage them. The development of periprocedural conduction disturbances can be explained by the proximity of the aortic valve with the conduction system. The atrioventricular (AV) node is located within the triangle of Koch in the right atrium and is in close proximity to the subaortic region and the membranous septum (MS). The AV node continues as the bundle of His and branches into the right and left bundle branch (RBB and LBB, respectively). The bundle of His is located in the MS and the LBB emerges at the level of the non-coronary aortic cusp, just below the posteroinferior MS edge. Thus, the length of the MS is equal to the distance between the aortic annulus and the exit point of the bundle of His. 8 This close relationship between the LBB and aortic cusp explains the predisposition to conduction disturbances after TAVI (Figure ).

Background: Pulmonary veins (PV) and the atria undergo electrical and structural remodeling in atrial fibrillation (AF). This study aimed to determine PV and left atrial (LA) reverse remodeling after catheter ablation for AF assessed by chest computed tomography (CT). Methods: PV electrophysiologic studies and catheter ablation were performed in 63 patients (68% male; mean ± SD age: 56 ± 10 years) with symptomatic AF (49% paroxysmal, 51% persistent). Chest CT was performed before and 3 months after catheter ablation. Results: At baseline, patients with persistent AF had a greater LA volume (91 ± 29 cm(3) vs. 66 ± 27 cm(3); P = 0.003) and mean PV ostial area (241 ± 43 mm(2) vs. 212 ± 47 mm(2); P = 0.03) than patients with paroxysmal AF. There was no significant correlation between the effective refractory period and the area of the left superior PV ostium. At 3 months of follow-up after ablation, 48 patients (76%) were AF free on or off antiarrhythmic drugs. There was a significant reduction in LA volume (77 ± 31 cm(3) to 70 ± 28 cm(3); P < 0.001) and mean PV ostial area (224 ± 48 mm(2) to 182 ± 43 mm(2); P < 0.001). Patients with persistent AF had more reduction in LA volume (11.8 ± 12.8 cm(3) vs. 4.0 ± 11.2 cm(3); P = 0.04) and PV ostial area (62 mm(2) vs. 34 mm(2); P = 0.04) than those who have paroxysmal AF. The reduction of the averaged PV ostial area was significantly correlated with the reduction of LA volume (r = 0.38, P = 0.03). Conclusions: Catheter ablation of AF improves structural remodeling of PV ostia and left atrium. This finding is more apparent in patients with persistent AF treated by catheter ablation.

An 83-year-old man with acute inferior wall myocardial infarction underwent successful percutaneous coronary intervention for right coronary artery. Subsequent echocardiography 3 days later showed an incidental huge cardiac chamber compressing left atrium. The chamber was found to have a narrow neck connecting with left ventricle, suggestive of a pseudoaneurysm. Real-time 3-dimensional echocardiography could clearly demonstrate the spatial relationship between pseudoaneurysm and corresponding cardiac chambers, and its precise location and the orifice of pseudoaneurysm. A myocardial break-out point resembling a bird beak with a flap could also be clearly seen and quantified by real-time 3-dimensional echocardiography. This patient underwent surgical resection and the serial follow-up remained uneventful. (J Am Soc Echocardiogr 2007;20:772.e5-e9.) From the Mackay Memorial Hospital.

Although the beneficial effect of sacubitril/valsartan (SAC/VAL) compared to enalapril was consistent across ischaemic cardiomyopathy (ICM) and non-ischaemic cardiomyopathy (NICM) groups, the PARADIGM-HF study did not analyse the effect of ventricular remodelling on patients with different aetiologies, which may affect clinical treatment outcomes. This study aimed to compare left ventricular ejection fraction (LVEF) following SAC/VAL treatment and its association with clinical outcomes.

The emerging data supports rhythm control to prevent major adverse cardiac events (MACE) in high-risk patients with atrial fibrillation (AF). Limited data demonstrated rivaroxaban 10 mg combining dronedarone seemed feasible. This study aimed at investigating clinical events in a dronedarone-treated cohort. This exploratory, retrospective chart review was conducted in nonpermanent AF patients receiving dronedarone for ≥ 3 months between 2009/1 and 2016/2. In Taiwan, dronedarone's labeled indication was strict to age ≥ 70 or 65 to 70 years with either hypertension, diabetes, prior stroke, or left atrium >50 mm. We divided all into 4 groups using antithrombotic strategies to evaluate the safety, effectiveness, and MACE endpoints. A total of 689 patients (mean CHA 2 DS 2 -VASc score 3.8 ± 1.4) were analyzed: rivaroxaban 10 mg (n = 93, 13.5%), warfarin (n = 89, 12.9%), antiplatelet (n = 331, 48.0%), and none (n = 176, 25.5%). During the follow-up period (mean 946 ± 493.8 days), the rivaroxaban group did not report any stroke or thromboembolism (ishcmeic stroke rate: antiplatelet [0.6%], none [1.1%]; hemorrahgic stroke rate: warfarin [2.2%]; thromboembolism rate: warfarin [2.2%]). There was no significant difference in safety, effectiveness, and MACE endpoints between groups. Also, >104 weeks of dronedarone use was the independent predictor for MACE after adjusting the strategy and other covariates (hazard ratio 0.14 [95% confidence interval 0.04-0.44], P = .001). Our findings warrant concomitant rivaroxaban 10 mg and dronedarone for further investigation. Regardless of antithrombotic strategies, a more extended persistence of dronedarone was associated with fewer MACE.

Background: In patients with frequent premature ventricular contractions (PVCs), little is known about the profile of PVCs and the outcome of treatment in patients with mitral valve prolapse (MVP) compared to those without MVP. Methods and results: Patients with documented PVCs between January 2001 and October 2012 were divided into 2 groups: MVP and non-MVP. The PVC characteristics, efficacy of therapy, and outcome were compared between the 2 groups. A total of 112 patients with MVP and 952 without MVP were identified. The frequency of PVCs was similar between the 2 groups (P N .05). In patients who underwent cardiac mapping, PVCs originating in papillary muscles (26.7% vs 2.3%; P b .001) and fascicle (13.3% vs 3.4%; P b .001) were more frequently seen in the MVP group than in the non-MVP group, which raises the difficulty of catheter ablation. The 2 groups had similar response to catheter ablation or medical therapy (P N .05). The survival rate was similar between the 2 groups (P = .95). In patients with significant PVC burden, MVP patients had similar PVC frequency, treatment outcome, and survival rate to those without MVP.

The current treatment paradigm for atrial fibrillation (AF) prioritizes rate control over rhythm control; however, rhythm control has shown benefits over other AF strategies. This study compares the outcomes of rivaroxaban with and without concomitant antiarrhythmic drugs (AADs), using propensity score matching to correct for statistical effects of baseline discrepancies. This multi-center retrospective study included 1,477 patients with non-permanent AF who took rivaroxaban for at least one month between 2011 and 2016 and had not received catheter ablation. Concomitant AAD use was compared against clinical outcome endpoints for effectiveness, safety, and major adverse cardiac events (MACE). Associations with concomitant AAD use were evaluated using multivariate Cox proportional hazard analyses. Patients were divided into two matched groups: rivaroxaban alone (n = 739) and with concomitant AADs (n = 738). The cumulative incidences of safety (p = 0.308), effectiveness (p = 0.583), and MACE (p = 0.754) were similar between the two groups, and multivariate analysis showed no significant differences. The new thromboembolism and all-cause death rates were higher in rivaroxaban alone (2.7% vs 0.8%, p = 0.005; and 10% vs. 6.9%, p = 0.032, respectively). The heart failure readmission rate was higher in the concomitant-AAD group (8.4% vs. 13.3%, p = 0.003). The concomitant use of rivaroxaban with AADs appears to be well-tolerated, with lower rates of thromboembolism and all-cause death, but is associated with more occurrences of congestive heart failure. The current treatment paradigm for atrial fibrillation (AF) prioritizes rate control over rhythm control, a direct result of large controlled trials, such as the AFFIRM trial from 2002, which concluded that, with regards to AF, there were no survival advantages to rhythm control over rate control and have further suggested that there may be advantages of rate control over rhythm control, such as lower rates of hospitalization and adverse drug effects 1 . However, rhythm control using dronedarone can reduce cardiovascular hospitalization or death and may be beneficial for stroke prevention, according to the ATHENA study and associated post-hoc analysis 2 . The EAST AFNET 4 trial investigators found that, compared with usual care, early initiation of rhythm-control therapy was associated with less-frequent cardiovascular events 3 . This early rhythm-control therapy included antiarrhythmic drugs, atrial fibrillation ablation, as well as cardioversion of persistent atrial fibrillation which were administered concomitantly with anticoagulants 3 . However, according the AFFIRM and ANDROMEDA

Cardiac implantable electronic devices (CIEDs) can measure atrial fibrillation (AF) early; however, the timing for administering antiarrhythmic drugs (AADs) to suppress AF remains unclear. This study aimed to investigate the association between baseline values and changes after AAD in terms of relative reduction of AF burden (RRAB) and maximum AF duration (RRMD). This multicenter retrospective study screened all patients with non-permanent AF who had dual-chamber pacemakers and only enrolled those receiving a naive AAD between September 2009 and December 2014. AF burden and maximum duration were calculated using CIED at 0 and 3-6 months after starting rhythm control. All the enrolled patients were divided into four groups according to baseline AF burden. RRAB and RRMD were monitored using CIEDs.

Sympathetic overactivity, an essential mechanism of hypertension, in driving sustained hypertension derives mostly from its effects on renal function. Percutaneous renal denervation (RDN) is designed to disrupt renal afferent and efferent sympathetic nerves to achieve sustained blood pressure (BP) reduction. Since 2017 onward, all three proof-of-concept, sham-controlled RDN trials demonstrated that RDN achieved consistent and clinically meaningful BP reductions [approximately 10 mmHg in office systolic BP (SBP) and 6-9 mmHg in 24-hour SBP] compared to sham operation in patients with mild to moderate or uncontrolled hypertension. There were no serious adverse events. The registry data in Taiwan showed similar 24-hour BP reductions at 12 months following RDN. The Task Force considers RDN as a legitimate alternative antihypertensive strategy and recommends 1) RDN should be performed in the context of registry and clinical studies (Class I, Level C) and 2) RDN should not be performed routinely, without detailed evaluation of various causes of secondary hypertension and renal artery anatomy (Class III, Level C). RDN could be performed in patients who fulfill either of the following BP criteria: 1) office BP ≥ 150/90 mmHg and daytime ambulatory SBP ≥ 135 mmHg or diastolic BP (DBP) ≥ 85 mmHg, irrespective of use of antihypertensive agents (Class IIa, Level B), or 2) 24-hour ambulatory SBP ≥ 140 mmHg and DBP ≥ 80 mmHg, irrespective of use of antihypertensive agents (Class IIa, Level B), with eligible renal artery anatomy and estimated glomerular filtration rate ≥ 45 mL/min/1.73 m2. Five subgroups of hypertensive patients are deemed preferred candidates for RDN and dubbed "RDN i2": Resistant hypertension, patients with hypertension-mediated organ Damage, Non-adherent to antihypertensive medications, intolerant to antihypertensive medications, and patients with secondary (2ndary) causes being treated for ≥ 3 months but BP still uncontrolled. The Task Force recommends assessment of three aspects, dubbed "RAS" (R for renal, A for ambulatory, S for secondary), beforehand to ascertain whether RDN could be performed appropriately: 1) Renal artery anatomy eligibility assessed by computed tomography or magnetic resonance renal angiography if not contraindicated, 2) genuine uncontrolled BP confirmed by 24-hour Ambulatory BP monitoring, and 3) Secondary hypertension identified and properly treated. After the procedure, 24-hour ambulatory BP monitoring, together with the dose and dosing interval of all BP-lowering drugs, should be obtained 6 months following RDN. Computed tomography or magnetic resonance renal angiography should be obtained 12 months following RDN, given that renal artery stenosis might not be clinically evident.

Background Cardiovascular disease shares several risk factors with type 2 diabetes. We tested whether the Finnish Diabetes Risk Score (FINDRISC), recently developed in a Finnish population to estimate the future risk of diabetes, would also identify individuals at high risk of coronary heart disease (CHD) and stroke, and total mortality in this same population. Design Independent risk factor surveys were conducted in 1987, 1992, and 1997 in Finland, comprising 8268 men and 9457 women aged 25-64 years and free of CHD and stroke at baseline. During the follow-up until the end of 2001, 699 incident acute CHD events, 324 acute stroke events, and 765 deaths occurred. Methods The data were analysed by using receiver operating characteristic (ROC) curves and the Cox-regression model. Results The areas under the ROC curves (AUC) were 71% for CHD, 73% for stroke, and 68% for total mortality in men and 78, 68, and 72% in women, respectively. The addition of systolic and diastolic blood pressu...

Aims To evaluate the joint associations of history of hypertension at baseline and type 2 diabetes at baseline and during follow-up on the incidence of coronary heart disease (CHD) and CHD mortality. Study cohorts included 49 775 Finnish subjects aged 25-74 without history of CHD and stroke. The multivariable-adjusted hazard ratios (HRs) of CHD incidence were 1. 25, 1.69, 1.25, 1.83, 1.85, 2.39, 2.15, and 3.31 (P-value for trend ,0.001), respectively, among men with hypertension I (blood pressure 140-159/90-94 mmHg or using antihypertensive drugs at baseline but blood pressure ,160/95 mmHg) only, with hypertension II (blood pressure 160/95 mmHg) only, with incident diabetes during follow-up only, with both hypertension I and incident diabetes, with both hypertension II and incident diabetes, with history of diabetes at baseline only, with both hypertension I and history of diabetes, and with both hypertension II and history of diabetes compared with men without either of these diseases. The corresponding HRs of CHD incidence among women were 1. 52, 2.37, 2.45, 3.78, 4.56, 5.63, 6.10, and 7.41 (P-value for trend ,0.001), respectively. The impact on CHD mortality associated with the different strata of hypertension and diabetes was almost the same or a little stronger compared with that on the CHD incidence. Conclusion Hypertension and type 2 diabetes increase the CHD risk independently, and their combination increases the risk dramatically, particularly in women.

A 26-year-old man with Ebstein's anomaly had cerebellar infarction due to paradoxical embolism. Ebstein's anomaly is characterized by a downward displacement of the tricuspid valve into the right ventricle due to anomalous attachment of the tricuspid leaflets. Echocardiography is the method of choice to diagnose Ebstein's anomaly on its own or in association with other heart defects. Paradoxical embolism is a potential complication whenever a right to left shunt exists (for example, atrial septal defect). Ebstein's anomaly diagnosed in adult life is a benign and stable disease, particularly if the patient is asymptomatic; surgical correction must be performed if the patient becomes symptomatic because of either paradoxical embolism or worsening of the tricuspid regurgitation.

A 52-year-old woman was admitted with the complaint of dyspnea that was present at rest and lasted a few hours. On bedside echocardiography, multiple small thrombus formations were detected in the right atrium under the tricuspid valve. Similar thrombus formation was detected in the left atrium. The lung perfusion scintigraphy indicated pulmonary embolism. Recombinant tissue plasminogen activator was started via intravenous infusion; after a dose of 60 mg, speech disturbance was observed, so thrombolytic therapy was terminated. The patient's speech problem subsided spontaneously. The dyspnea improved dramatically. Repeated bedside echocardiographic examination revealed the thrombi in both atria had disappeared. (ECHOCARDIOGRAPHY, Volume 15, August 1998) biatrial thrombi, pulmonary embolism, thrombolytic therapy Atrial thrombosis is one of the most common causes of pulmonary thromboembolism. Two-dimensional (2-D) echocardiography has a major role in detecting left atrial thrombosis with a 70%-90% sensitivity and 98% specificity. The sensitivity of 2-D echocardiography is very low for the diagnosis of the left atrial thrombosis localized at the appendix, but for the right atrial thrombosis, which occurs more rarely, it is a

Siblings, a 26-year old male and a 31-year old female, were found do have Ebstein&#39;s anomaly. Ebstein&#39;s anomaly is characterized by a downward displacement of the tricuspid valve into the right ventricle due to anomalous attachment of the tricuspid leaflets. Echocardiography is the method of choice to diagnose Ebstein&#39;s anomaly on its own or in association with other heart defects.

The value of dobutamine echocardiography and 99mTc-sestamibi SPECT imaging was evaluated as a noninvasive diagnostic method for assessing coronary artery disease (CAD). Twenty-seven patients who underwent coronary angiography were submitted to two separate injections of 99mTc-sestamibi, one under control conditions and the other after reaching a peak dobutamine infusion rate. Simultaneous ECG and echocardiographic monitoring was also performed during stepwise dobutamine infusion. Whereas the overall sensitivity and specificity of dobutamine sestamibi SPECT imaging were 94% and 88%, these values for dobutamine ECG and echocardiography were 61%, 55% and 84%, 88%, respectively. When dobutamine echocardiography and 99mTc-sestamibi SPECT imaging were evaluated together, the diagnostic accuracy reaches almost 100%. Dobutamine echocardiography is of value in determining ischemic threshold earlier than clinical symptoms and allows simultaneous evaluation of ventricular performance and contr...

Background: Remote monitoring of heart failure (HF) patients (pts) enables proactive detection of condition worsening and titration of medical therapy. Although current methods use indirect physiologic assessment (e.g. bodyweight, thoracic impedance) or measurements of pulmonary artery pressures at rest, no method exists to monitor cardiac contractility or its response to activity. Objective: We hypothesized that the degree of impairment in myocardial contractility after exercise will be able to differentiate compensated from decompensated HF pts. We developed a wearable patch (Fig. ) that measures electrocardiogram (ECG) and ballistocardiogram (BCG) signals, and can compute-from the time delay between the peaks of these signals (Fig. )-an index of myocardial contractility based on the pre-ejection period (PEP). We hypothesized that changes in PEP following a standardized six minute walk test (6MWT), would be significantly different between decompensated HF pts [New York Heart Association (NYHA) class IV] as compared to stable, compensated HF patients (NYHA class I-II). Methods and Results: We recruited 21 pts (9 NYHA class I-II and 12 NYHA class IV, 24% women, ejection fraction 0.29 ± 0.17), and measured ECG and BCG signals with our wearable patch during a 6MWT. For each pt, we computed the percent (%) changes in PEP following the test (normalized to their baseline PEP value at rest), as well as the % predicted value of the 6MWT distance (based on age, height, weight, gender). The changes in PEP were significantly lower for the NYHA class IV compared to the NYHA class I-II pts (Fig. , P < .05). As expected, we also found a significant difference in both distance walked and % predicted 6MWT distance between the two groups (369 ± 74 m, 79 ± 25% predicted for NYHA class I-II vs. 207 ± 70 m, 36 ± 11% predicted for NYHA class IV, P < .01). We did not find any significant differences in the heart rate response in the two groups, supporting the importance of measuring a combination of electrical and mechanical signals from the heart (i.e., ECG and BCG). Conclusions: While the 6MWT requires pts to perform a prescribed activity, changes in PEP can be observed in response to any natural activity that pts perform on their own while wearing the patch. In fact, since the BCG measurement is based on accelerometry, the patch can quantify both the changes in PEP and the level/ distance of activity performed in natural settings. This approach may increase HF pts adherence as it will require less regimented testing, while providing an indication of condition worsening or improving.

To determine the frequency of hyperhomocysteinemia level in patients with ischemic heart diseases. Study Design: Case series study. Setting: Liaquat University Hospital Hyderabad. Period: Six months. Patients and Methods: All the patients with known ischemic heart disease of either sex gave the history of myocardial infarction and echocardiography showed motion wall abnormalities were recruited and entered in the study. After confirmation of IHD, the 2cc venous blood sample was taken in sterilize disposable syringe and sent to laboratory for evaluation of serum homocysteine levels while the data was collected on pre-designed proforma and the data was analyzed in SPSS 16 and the frequency and percentage was calculated. Results: Total one hundred patients with known ischemic cardiac disease were recruited and evaluated for homocysteine level. The mean ±SD for age of patients with ischemic heart diseases was 55.82±10.94. Majority of the patients were males 57% and the male to female cross tabulation was statistically significant (p=0.02). The hyperhomocysteinemia was not statistically significant in relation to age while it is significant in relation to gender (p=0.01). The overall frequency of hyperhomocysteinemia in IHD was 62% with male predominance 66%, of sixty percent hyperhomocysteinemic individuals 41.9% had severe, 37.1% had intermediate and 21% had mild elevated homocysteine level (p=0.02). It was concluded that hyperhomocysteinemia was associated with ischemic heart disease (62%) with advance age and male gender predominance (66%).

To determine the electrocardiographic and echocardiographic findings in patients with acute ischemic stroke (potential source of cardiac emboli). Study Design: Cross section descriptive study. Period: Six months. Setting: Liaquat University Hospital Hyderabad. Patients and Methods: The subjects with history and clinical features suggestive of cerebrovascular accident (CVA). After establishing the diagnosis of acute ischemic stroke the electrocardiography (ECG) was advised and those subjects had abnormal findings on ECG were went for echocardiography to evaluate the specific cause related to acute ischemic stroke. The two-dimensional and M-mode echocardiography was performed by consultant cardiologist had ≥ five years experienced in echocardiography because echocardiographic study in patients with cerebrovascular accident (confirmed on CT scan) is evidence of potential cardiac abnormalities as a predisposing cause for the vascular event. The data was collected on pre-designed proforma and was analyzed in SPSS 16 and the frequency and percentage was calculated. Results: Total one hundred patients with acute ischemic stroke were studied for electrocardiographic and echocardiographic findings during six months study period. The mean ±SD for age of patients with acute ischemic stroke was 43.67±10.62. Majority of the patients were males and 69% while the age and gender cross tabulation was also statistically significant (p=0.03). The electrocardiographic abnormalities were indentified in 80% patients (AF in 16.2%, LVH in 22.5%, LBBB in 10%, wide QRS complex in 10% and ischemic changes in 8.7%) while the echocardiographic abnormalities were detected in 70% patients of which global hypokinesia (28.5%), LVH (25.7%) and diastolic dysfunction (17.14)% were predominant. The cardiac embolic source is the major cause for acute ischemic stroke and detected by echocardiography as it is the main tool in diagnosing the source of embolus.